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• Treatment:
• Factor IX concentrate (available for
home administration)
• Hemophilia C (Factor XI deficiency)
• Hemophilia C or Plasma thromboplastin
antecedent deficiency)
• Autosomal recessive trait affecting both
sexes
• Mild symptoms compared to patients with
Factor VIII or Factor IX deficiencies
• Treatment:
• Administration of arginine desmopressin
(DDAVP) – vasoconstricting agent, blood
transfusion or plasma
• Hyperbilirubinemia
• Occurs on the 2nd or 3rd day of life in
about 50% of cases as a result of
breakdown of fetal RBC.
• 7 mg/100 ml. –hyperbilirubinemia
• If intestinal obstruction is present;
intestinal flora may break down bile
into its basic components leading to the
release of indirect bilirubin in the
bloodstream
• Early feeding helps prevent build up of
indirect bilirubin
• Serum bilirubin is obtained by heel puncture
• If level rises above 10-12 mg/100 ml
treatment is considered
• 20 mg/100 ml could interfere with the
chemical synthesis of brain cells, resulting
to permanent brain damage called
Kirnecterus
• Treatment for physiologic jaundice is
rarely necessary except for early
feeding (to speed passage of feces
through the intestine & prevent
reabsorption of bilirubin from the
bowel)
• Phototherapy – exposure of infant to
light to initiate maturation of liver
enzymes
• Breastfed babies have a little
difficulty in converting indirect
bilirubin to direct bilirubin due to
pregnanediol (metabolite of
progesteron) – depresses the action
of glucoronyl transferase
Breakdown of Fetal
RBC
Heme Globin
Protoporphy
Iron
rin
Direct Bilirubin
(Water Soluble)
Indirect Bilirubin
Immature Hyperbilirubine
Glucoronyl mia Jaundice
Transferase (7 mg./100 ml)
Kirnecterus
(20 mg/100 ml)
Permanent
brain damage